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SnoRNA:U3:9B is required for the activation of immune response genes in Drosophila melanogaster [RNA-Seq]

ABSTRACT: Small nucleolar RNAs (snoRNAs) are prevailing components of the chromatin-associated transcriptome. We have studied a specific chromatin-associated snoRNA, snoRNA:U3:9B, that binds to a large number of protein coding genes in the genome of Drosophila melanogaster, including immune response genes. We have used CRISPR/Cas9 to delete snoRNA:U3:9B. SnoRNA:U3:9B-deficient larvae were viable in control conditions but failed to develop into pupae when challenged by expression of a Sindbis virus replicon, which suggests that snoRNA:U3:9B is required for the activation of an effective antiviral response. Consistent with this hypothesis, the chromatin decompaction and gene activation typically observed at immune response genes in response to Sindbis replicon expression were abolished in snoRNA:U3:9B-deficient larvae. Moreover, snoRNA:U3:9B was required for the recruitment of the ATP-dependent helicase brm to a set of target immune genes. The association of snoRNA:U3:9B with immune response genes in vivo shown by ChIRP-qPCR suggests that the chromatin and gene expression defects observed in the snoRNA:U3:9B knock-out strains are due to direct regulatory events. In summary, our findings reveal an immune defence mechanism that relies on a snoRNA for the recruitment of chromatin remodelling factors to immune genes, thereby modulating local chromatin accessibility to facilitate immune gene activation.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE281409 | GEO | 2025/07/29

REPOSITORIES: GEO

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Project description:Osteoarthritis (OA) is a chronic debilitating joint disease which is strongly associated with ageing. OA involves pathological cellular processes in all joint structures and affects articular cartilage integrity, leading to dysfunctional joint articulation. The biomolecular processes that catalyze the disturbances in the articular chondrocyte phenotype leading to OA are poorly understood, and it is expected that a comprehensive understanding of the avenues leading to catabolic changes and disruption of articular chondrocyte homeostasis will provide important cues for future treatments of the condition. Chondrocytes are specialized secretory cells with highly active protein translational machinery, enabling the synthesis and maintenance of the protein-rich cartilage extracellular matrix (ECM). Disturbances in chondrocyte protein translation in cartilage development and OA are connected to mTOR activity, ER stress, unfolded protein response (UPR)and CHOP-mediated apoptosis. These responses change the downstream translational activity of the biosynthesized ribosome. The assembled mammalian ribosome is built from ribosomal RNAs (rRNAs), together with more than 80 different protein subunits. At the heart of the ribosome, the 18S rRNA guides the decoding of the mRNA message, while an ancient ribozyme activity in the 28S rRNA forms the core of the peptidyltransferase center that polymerizes the amino acid sequence encoded by the mRNA into functional proteins. Post-transcriptional maturation of rRNAs is an integral part of the biosynthesis of ribosomes and ribonucleolytic processing of the major 47S rRNA precursor into mature 18S, 5.8S, and 28S rRNAs is rate limiting for ribosome biogenesis. The U3 small nucleolar RNA (snoRNA) is an evolutionarily highly conserved box C/D-class snoRNA which catalyzes the endoribonucleolytic processing of the 5’ external transcribed spacer (ETS) of the 47S pre-rRNA by base complementarity-guided pre-rRNA substrate recognition and plays a crucial role in the maturation of 18S rRNA. Although extensively studied in yeast, it was only recently demonstrated that U3 snoRNA is indispensable for rRNA maturation in human cells. Pathways controlling ribosome activity have previously been described in the regulation of chondrocyte homeostasis. We here now postulate that not only ribosome activity is involved in chondrocyte homeostasis, but that OA pathophysiological situations can also cause alterations in chondrocyte ribosome biogenesis with consequences for cellular protein translation. Since U3 snoRNA-driven rRNA production is rate-limiting in ribosome biogenesis, we hypothesized that the U3 snoRNA is critical for chondrocyte homeostasis. In this study we therefor aimed to determine whether OA pathophysiological conditions interact with chondrocyte U3 snoRNA levels, thereby influencing rRNA levels and chondrocyte translation capacity.

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SnoRNA:U3:9B is required for the activation of immune response genes in Drosophila melanogaster [RNA-Seq]

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